The present invention relates to medicinal treatment, and more particularly, to medicinal treatments and preventions to treat herpes, pseudomonas, staphylococcus (staph), and hepatitis and help treat or alleviate cold sores, rashes, skin conditions, or symptoms resulting from herpes, pseudomonas, staph, and hepatitis.
Cold sores, also known as fever blisters, are clusters of small blisters on the lip and outer edge of the mouth. They are called cold sores or fever blisters because they often occur during a viral illness, such as a cold. Cold sores are small, painful, fluid-filled blisters on the mouth or nose. The skin around the blisters is often red and inflamed. The blisters can break open, weep a clear fluid, and then scab over after a few days. Cold sores usually appear on the lips. Occasionally, they occur on the nostrils, chin or fingers. Sometimes, cold sores can occur inside the mouth, but typically on the gums or hard palate or roof of the mouth.
Cold sores are caused by a viral infection or a virus known as herpes simplex type I (HSV-1) that attacks the skin and nervous system. Cold sores are the most common manifestation of a herpes simplex virus infection. Fever blisters are caused more often by the herpes simplex virus type 1 (HSV-1) than herpes simplex virus type 2 (HSV-2). HSV-1 is different from herpes simplex type II (HSV-2), which is the virus that causes the sexually transmitted disease known as genital herpes. Herpes simplex virus type 2 is usually responsible for genital herpes. However, either type of the herpes virus can cause sores in the facial area or on the genitals.
After the first episode of cold sores or fever blisters, the herpes virus lies dormant in the nerves or skin around the original area until something sets the virus off into another eruption. Herpes simplex virus can be reactivated in response to various stimuli including UV radiation from sun exposure, stress, a cold, illness, or dental work. Fever and menstruation can also trigger a recurrence of cold sores.
Cold sores or fever blisters are contagious and can be spread by direct contact with infected saliva or droplets in the breath, or by skin to skin contact. Cold sores can be spread through coughing, sneezing, direct contact with a cold sore, or touching contaminated fluid-such as from kissing an infected person and touching the person's saliva. Cold sores can also be spread from one person to an area of someone else's body by touching an active cold sore or sharing things that a person who has a cold sore has used. Shared eating utensils, razors and towels can spread the infection of cold sores. A parent who has a cold sore can spread the infection to their child. The greatest risk of infection of cold sores is from the time the blisters appear until they have completely dried and crusted over. There is a possibility of spreading the virus from cold sores even after the skin has healed.
People with cold sores should avoid close contact with infants, anyone who has eczema (atopic dermatitis) or people with a suppressed immune system, such as people with cancer, AIDS or an organ transplant. These people are at higher risk of more severe infection.
If the sore appears on the soft tissues inside the mouth, it may be a canker sore. Cold sores or fever blisters and are quite different from canker sores, a condition people sometimes associate them with. Cold sores are caused by the herpes simplex virus and they're contagious. Canker sores, which aren't contagious, are ulcers that occur in the soft tissues inside your mouth, places where cold sores don't occur. Cold sores are common occurrences although cold sores may not be completely curable or prevented, medicinal treatments can help reduce their frequency and limit the duration of their occurrence.
Complete healing of cold sores or fever blisters can take 7 to 10 days or more. For some people, however, cold sores can be painful. Initial symptoms can include mouth soreness, fever, sore throat, or swollen lymph glands. Small children sometimes drool before a cold sore appears. After the blisters develop, cold sores usually break open, weep clear fluid, and then crust over and disappear after several days to a week.
Cold sores follow the usual course of herpes simplex virus infections in that the first outbreak is usually more painful and lasts longer than recurrent infections. The first time the skin in or around the mouth comes in contact with the herpes simplex virus; the outbreak occurs inside the mouth on the gums, tongue, and throat. This is called gingivostomatitis. This first infection occurs most often in childhood, and the highest incidence of infection occurs between 6 months and three years of age. Children get pain, fever, swollen lymph nodes, and can have difficulty swallowing. These symptoms last for about a week and resolve spontaneously. Children with gingivostomatitis are at risk for dehydration if the pain keeps them from drinking fluids.
Once a person has been exposed to the herpes simplex virus, the virus remains in the cells in the body and can reactivate at any time. Reactivation can be triggered by trauma to the skin, menstruation, sun exposure, stress, fever, and other causes. This reactivation produces the lesions we know as cold sores or fever blisters. Fever blisters are most often seen on the border of the lip and consist of three to five vesicles. Over the next three to five days, the vesicles can become pustular, ulcerative, and then crust over. Symptoms are usually most severe 8 hours after the outbreak. Many people have about two outbreaks per year, but some people have greater than six outbreaks per year.
Recurrent infections of cold sores are often preceded by a prodrome, symptoms that appear before the outbreak occurs. Common prodromal symptoms for cold sores or fever blisters are pain, tingling, and burning. A herpes prodrome can last from two hours to two days. The first symptoms that can appear during an outbreak of cold sores may include tingling, burning, or itching in the area around the mouth or nose. This first portion of the outbreak is known as the prodromal stage or period. Within a few hours to days, the area may become reddened and develop small fluid-filled blisters. Several of these small blisters may even come together and form one large blister.
Signs and symptoms of cold sores can include: small, painful, fluid-filled blisters on a raised, red, painful area of the skin. Pain or tingling, called the prodrome, often precedes the blisters by one to two days. Signs and symptoms may not start for as long as 20 days after exposure to the herpes simplex virus, and usually last seven to 10 days. The blisters form, break and ooze. Then a yellow crust forms and finally sloughs off to uncover pinkish skin that heals without a scar.
Once a person has had an episode of cold sores, the virus lies dormant in the nerve cells in the skin and may emerge again as an active infection at or near the original site. The person may experience an itch or heightened sensitivity at the site preceding each attack.
The herpes simplex virus that causes cold sores cannot be cured. If sores develop regularly, treatment can reduce the number and severity of outbreaks. Herpes simplex infection of the eye can cause scarring of the cornea and is a leading cause of blindness in the United States.
Herpes simplex virus (HSV) commonly referred to as “herpes virus” or “herpes,” is an infectious disease which also has reached crisis proportions nationally with estimated numbers of infected people at 70%-80% of our population as reported by the American Societal Health Association (ASHA) and growing annually by 500,000 people. There are two common types of herpes: herpes simplex virus 1 (HSV 1) and herpes simplex virus 2 (HSV 2). Herpes enters the human body through minuscule breaks in the epidermal tissue usually by contact with an infected host and is marked by eruption of one or more vesicles, usually in groups, following an incubation period of approximately four days. Typically the course of the infectious outbreak initiates with the prodromal stage; advancing to vesicular eruption; followed by ulceration; coalescing; resolution; and the latency period. The outbreak can last for several weeks and on average lasts two-three weeks. In some immune compromised individuals the outbreak can last for months. The vesicles can appear anywhere on the skin or mucosa, typically appearing on the lips as cold sores, glands, oral mucosa, conjunctiva and cornea, genitalia, anal mucosa and peri-anal tissue.
Herpes symptoms include: inguinal swelling, pain, fever, malaise, headaches, muscle aches, and swollen glands. Some individuals who have the trigeminal nerve compromised with oral herpes, have excruciating facial pain, difficulty swallowing, eating and facial swelling. Individuals with the sacral nerve affected have severe upper leg pain, swelling, and great difficulty walking.
Herpes simplex virus (HSV) infection is recrudescent, residing in the nerve ganglia, and then recurring due to some, as yet unknown, stimulus. Recurrent herpetic infections can be precipitated by almost anything, including: overexposure to sunlight; nutritional deficiencies; stress, menstruation; immunosuppression; certain foods; drugs; febrile illness; etc. Herpes virus can be isolated from cardiac tissue.
HSV 1 and HSV 2 infections pose very serious health threats and can cause causing: blindness; increased cancer risk of the cervix; aseptic meningitis and encephalitis; neonatal deaths; viremia; etc. The devastating effects of this disease go well beyond the medical scope of human suffering. HSV is responsible for serious psychological and emotional distress as well as substantial economic loss to the nation and the world.
Various treatments for herpes have been proposed and have included topical application of such agents as povodone-iodine, idoxuridine, trifluorothymidine, or acyclovir. Such treatments have met with varying degrees of success. Most prior treatments have proven disappointing. Acyclovir, taken orally for systemic treatment of HSV, is somewhat effective. However, acyclovir is only successful in interrupting the replication of the virus. It is not successful in treating an infectious outbreak either systemically or topically. Strains resistant to acyclovir have been reported. Individuals with Auto Immune Deficiency Syndrome (AIDS) are seriously immune-compromised and suffer especially debilitating outbreaks of HSV. Additionally, AIDS individuals may carry acyclovir resistant strains of HSV, which can make acyclovir ineffective for these individuals.
It has been reported that there are currently about 22 million people infected with human immunedeficiency virus (HIV) throughout the world. The largest proportion of new HIV cases has originated in Africa and the Caribbean. The typical progression of HIV infection is divided into different stages: 1) viral transmission; 2) acute retroviral syndrome; 3) seroconversion; 4) a clinical latent period with or without persistent generalized lymphadenopathy (PGL); 5) early symptomatic HIV infection previously known as AIDS-related complex or ARC and more recently referred to as “B symptoms” according to the 1993 CDC classification); 6) acquired immune deficiency syndrome (AIDS) (AIDS indicator condition according to the 1987 CDC criteria and revised 1993 CDC criteria that include a CD4 cell count <200/mm3); and 7) advanced HIV infection characterized by a CD4 cell count <50/mm3. CD4 cells are lymphocytes targeted by HIV. In 1993 the CDC changed the definition of AIDS to include all patients with a CD4 count <200/mm3; this definition includes patients in stages 4-7 regardless of symptoms.
The initial acute retroviral syndrome is accompanied by a precipitous decline in CD4 cell counts, high culturable plasma viremia, and high concentrations of HIV RNA in plasma. Clinical recovery occurs and high level HIV RNA plasma viremia is reduced with development of cytotoxic T lymphocyte (CPL) response. The CD4 cell count gradually declines over several years and then shows an accelerated decline at 1.5-2 years before an AIDS-defining diagnosis. HIV RNA concentrations in plasma are relatively stable until the HIV is in a late stage when the CD4 count is <200/mm3 and the clinical course is characterized by infections, selected tumors, wasting, and neurological complications. Generally, about 10% of patients develop an AIDS-defining diagnosis before the CD4 count decreases to 200/mm3. The present median time to an AIDS-defining complication after the CD4 count is 200/mm3 is 12-18 months. In the absence of therapy directed against HIV or PCP prophylaxis, the average time from viral transmission to an AIDS-defining diagnosis is about 10 years, and survival after an AIDS-defining complication was previously about one year.
The entire sequence of events for an average patient, in the absence of treatment directed against HIV, is approximately ten years from seroconversion to death. The median time from HIV seroconversion to AIDS has been reported to be about 7 years for transfusion recipients, 10 years for hemophiliacs, 10 years for drug users and 8-12 years for gay men. Rates of progression appear similar by sex, race, and risk category if adjusted for quality of care. For patients aged 16-24 years at seroconversion, the median time was 15 years; for those over 35 years at seroconversion, it was 6 years.
HIV infection can be acquired through sexual intercourse, from drug transfusions with contaminated blood, by drug addicts with infected needles, or by prenatal transmission. Symptomatic primary HIV infection, also referred to as an acute retroviral syndrome, has been reported in the preceding risk categories with a frequency of 50-90%. This syndrome has also been noted in seven of eight healthcare workers with HIV transmission following occupational exposure. The time from exposure to onset of symptoms is usually 2-4 weeks, but the incubation may be as long as six weeks. Typical symptoms are: fever, adenopathy, pharyngitis, rash comprising erythematous maculopapular with 5-10 mm lesions on the face and trunk, sometimes extremities including palms and soles or mucocutaneous ulceration on the mouth, esophagus or genitals, myalgias or arthralgias, diarrhea, headache, hepatosplenomegaly, thrush, nausea and vomiting. Neurologic symptoms can include: meningoencephalitis, peripheral neuropathy, facial palsy, Guillain-Barré syndrome, brachial neuritis, radiculopathy, cognitive impairment, and psychosis. The acute illness is generally accompanied by high level HIV viremia with p24 antigenemia, plasma viremia, and high titers of HIV in peripheral blood mononuclear cells.
The cytotoxic T lymphocyte (CTL) response is first and usually precedes detectable humoral response by several weeks. CTL response is accompanied by a 3-5 log decrease in HIV concentration in peripheral blood. The high level of viremia during this acute phase of the illness may be associated with dissemination of the virus to the CNS and lymphatic tissue. Lymph tissue serves as the major reservoir of HIV burden and replication. Infection of non-lymphoid organs with high levels of HIV appears to occur in late-stages of HIV.
The presence of symptoms rather than asymptomatic seroconversion as well as a prolonged illness greater than 14 days appear to correlate with more rapid progression to AIDS. Seroconversion with positive HIV serology generally takes place at 6-12 weeks following transmission such as by transfusion or needles injury to a healthcare worker. The median interval is 63 days. The CTL response is associated with a sharp reduction in quantitative viral load in blood, clinical recovery from the acute retroviral syndrome and return of the CD4 cell count to higher levels that are often in the normal range for most laboratories.
The HIV patient becomes clinically asymptomatic and generally has no findings on physical exam except for Persistent Generalized Lymphadenopathy (PGL) comprising enlarged lymph nodes. Studies of lymph nodes show high concentrations of HIV as extracellular virus trapped on the follicular dendritic cell processes within germinal centers and as intracellular virus predominantly in latent form. The lymph tissue serves as a major reservoir for HIV, the follicular dendritic cells filter and trap free virus and infected CD4 cells, and the viral burden in peripheral blood mononuclear cells is relatively low. With progressive disease, the lymph node configuration is disrupted by HIV.
Virologic studies in patients with asymptomatic HIV infection show high rates of HIV replication with production of an average of 109 virions daily. Viral replication is accompanied by massive destruction and the production of 109 CD4 cells daily. The turnover of CD4 cells represents 6-7% of the total body CD4 cells so that the entire supply turns over every 15 days. AIDS has been considered a consequence of continuous, high-level replication of HIV-1, leading to virus and immune-mediated termination of CD4 lymphocytes.
Advanced HIV Infection occurs in patients with a CD4 cell count of <50/mm3. These patients have limited life expectancy with a median survival of 12-18 months. Virtually all patients who die of HIV-related complications are in this CD4 cell count stratum.
The Food & Drug Administration (FDA) has approved many reverse transcriptase (RT) inhibitors. RT enzymes convert viral RNA into DNA. RT inhibitors can interrupt this process. The RT inhibitor AZT, which is sold under the brand names of Retrovir and zidovudine by Glaxo Wellcome, was approved by the FDA in 1987. The RT inhibitor ddl, which is sold under the brand names of Videx and didanosine by Bristol-Myers Squibb, was approved by the FDA in 1991. The RT inhibitor ddC, which is sold under the brand names of HIVID and dideoxycyytidine by Hoffman-LaRoche, was approved by the FDA in 1992. The RT inhibitor d4T, which is sold under the brand names of Zerit and stavudine by Bristol-Myers Squibb, was approved by the FDA in 1994. The RT inhibitor 3TC, which is sold under the brand names of Epivir and lamivundine by Glaxo Wellcome, was approved by the FDA in 1995. The TR inhibitor Nevirapine, which is sold under the brand name of Viramune by Boehringer Ingelheim, was approved by the FDA in 1996.
The Food & Drug Administration (FDA) has now approved three protease inhibitors for the treatment of human immunedeficiency virus (HIV) infection. Saquinavir sold under the brand name of Invirase by Hoffman-LaRoche Laboratories, was the first protease inhibiting agent to be approved by the FDA. Ritonavir, another protease inhibitor, which is sold under the brand name of Norvir by Abbott Laboratories, received FDA approval in March, 1996 as did Indinavir sold under the brand name of Crixivan by Merck & Co.
Protease inhibitors have a different mechanism of action from that of previously approved anti-HIV drugs, such as the nucleoside analogues AZT and 3TC sold under the brand names of zidovudine and lamivundine by Glaxo Wellcome, ddl and d4T sold under the brand names didanosine and stavudine by Bristol-Myers Squibb, and ddC sold under the brand name of dideoxycytidine by Roche Laboratories. Protease inhibitors block the enzyme which HIV requires for the completion of its replication cycle and formation of viable new viruses. Without the protease enzyme, viral structural proteins cannot be manufactured properly, and faulty, non-infectious virus is formed. The nucleoside analogues block a different enzyme-reverse transcriptase. This action can prevent viral RNA from producing viral DNA which can then incorporate into the DNA of human cells. Combining one or more reverse transcriptase inhibitors with a protease inhibitor, sometimes referred to as a “cocktail,” is claimed to attack HIV replication at two points in the replication cycle. Clinical trials combining saquinavir with AZT, ddC, or both demonstrate a greater decline in the number of HIV particles in the blood, sometimes referred to as viral burden, and a grater increase in CD4 cells (T lymphocytes) than previously observed with reverse transcriptase inhibitors alone. Sometimes, the cocktails have been toxic and ineffective for some patients. Clinical benefit in terms of improved survival or reduced disease progression rate, however, has not yet been fully demonstrated for combination (cocktails) of RT inhibitors and protease inhibitors. Physicians, however, are starting to consider HIV a chronic manageable disease rather than a death sentence.
Saquinavir protease inhibitors have been approved by the FDA for use in combination with reverse transcriptase inhibitors in patients with advanced AIDS. Saquinavir protease inhibitors may be tolerated by some patients without the hematologic or neurologic toxicities encountered with the nucleoside analogues. Certain prescription drugs including rifampin, rifabutin, phenobarbital, dilantin, and dexamethasone, may significantly decrease plasma levels of saquinavir protease inhibitors and should be avoided in patients taking saquinavir. Viral resistance to saquinavir protease inhibitors, as with other anti-HIV drugs has been reported.
Ritonavir and indinavir protease inhibitors appear to be more potent against HIV than the current formulation of saquinavir. Ritonavir protease inhibitors require refrigeration. Ritonavir protease inhibitors are currently used in combination with nucleoside analogues (drugs like AZT) or as monotherapy. An early study treated 32 patients with ritonavir plus AZT plus ddC. After 20 weeks, median CD4 cell counts rose from 83 cells/mm3 at baseline to 106 cells/mm3. Viral load, a measure of the number of viral copies in the blood, decreased by almost 100-fold. Ritonavir is dosed at 600 mg orally twice a day, which can require twelve capsules each day. The drug is available in 100 mg capsules. Side effects are fairly common, including: gastrointestinal symptoms with nausea, vomiting, and diarrhea. Other side effects include numbness and tingling, particularly around the mouth, and liver inflammation comprising a form of hepatitis.
Indinavir protease inhibitors received accelerated FDA approval based on studies demonstrating mean rises in CD4 counts of about 100 cells/mm3 and drops in viral load of almost 100-fold with a combination of AZT plus 3TC plus indinavir. Indinavir is dosed at 800 mg orally three times per day (2 capsules 3, times daily). In contrast to ritonavir, indinavir can be taken on an empty stomach to improve absorption. Indinavir causes fewer gastrointestinal side effects than ritonavir and seems to be better tolerated overall by some patients. The major side effect of Indinavir protease inhibitors are the development of kidney stones. The drug is partially excreted in the urine and it can crystallize to form stones if adequate hydration is not maintained. Indinavir protease inhibitors can also affect the liver, causing a rise in blood levels of bilirubin, i.e., a bile pigment formed from the breakdown of red blood cells. Indinavir protease inhibitors can also cause drug interactions.
Analysis of resistance to protease inhibitors has not been fully determined. Saquinavir and ritonavir protease inhibitors can currently cost the patient approximately U.S. $600 per month. Indinavir protease inhibitors is priced about 30% below this level. A three-drug combination of AZT plus 3TC plus ritonavir protease inhibitors can cost a patient over U.S. $1,000/month. Combinations (cocktails) of RT inhibitors and protease inhibitors can cost as much as $25,000 per year. Although, protease inhibitors may be helpful, the medical community and society have not yet resolved patient cost problems for these expensive drugs.
Staphylococcus is a group of bacteria, also known as Staph or staph (pronounced “staff”), that can cause a multitude of diseases as a result of infection of various tissues of the body. Staphylococcus is a genus of nonmotile gram-positive spherical eubacteria of the family Micrococcaceae that occur singly, in pairs or tetrads, or in irregular clusters and can comprise parasites of skin or parasites of mucous membranes. Staphylococci are the plural of Staphylococcus. 
Staph (Staphylococcus) is usually on a person's skin or in their nose or throat. Most of the time, the Staphylococcus bacteria cause no problems or relatively minor skin infections. When the skin is punctured or broken, staph bacteria can enter the wound and cause infections. When staph bacteria enter the bloodstream and spread to other organs, a number of serious infections can occur.
The name Staphylococcus comes from the Greek staphyle meaning a bunch of grapes and kokkos meaning berry, and that is what staph look like under the microscope, like a bunch of grapes or little round berries. Over 30 different types of Staphylococci (staph) can infect humans, but most infections are caused by Staphylococcus aureus. 
Staph bacteria cause skin infections, including boils; cellulites, a potentially life-threatening infection that leaves skin inflamed and tender; impetigo, a rash common in young children and infants; and scalded skin syndrome, a serious, blistering condition that mainly affects newborns. Though each condition has specific features, most begin with skin redness, swelling, warmth, tenderness and sometimes fever. Some staph infections are localized; others can cover your entire body.
Staph bacteria can cause illness not only directly by infection such as in the skin, but also indirectly by producing toxins. Staph-related illness can range from mild and requiring no treatment to severe and potentially fatal. However, staph infections can turn deadly if the bacteria burrow deeper into the body, invading the bloodstream, urinary tract, lungs, and/or heart. In the past, most lethal staph infections occurred in people who were hospitalized or had a chronic illness or weakened immune system.
Staph infections can range from minor skin problems to food poisoning, fatal pneumonia, surgical wound infections and endocarditis, a life-threatening inflammation of the heart lining. As a result, signs and symptoms of staph infections vary widely, depending on the location and severity of the infection and on whether the illness results from direct infection with staph bacteria or from toxins the bacteria produce, but most infections are accompanied by fever, chills and sweating.
Staphylococci or staphylococcus (staph) can be found normally in the nose and on the skin many healthy adults. In the majority of cases, the bacteria do not cause disease. However, damage to the skin or other injury may allow the bacteria to overcome the natural protective mechanisms of the body, leading to infection. Anyone can develop a staph infection, although certain groups of people are at greater risk, including: patients in hospitals, newborn infants, breastfeeding women, and people with chronic conditions such as diabetes, cancer, vascular disease, and lung disease. Drug users, people with skin injuries or disorders, intravenous catheters, surgical incisions, and people with a weakened immune system all have an increased risk of developing staph infections.
Staphylococcal disease (staph) of the skin usually results in a localized collection of pus, known as an abscess, boil, or furuncle. The area of the skin affected by staph can become red, swollen, and painful. Staph infections of the skin can progress to impetigo causing a crusting of the skin or cellulites causing inflammation of the connective tissue under the skin and leading to swelling and redness of the area. In some cases, a serious complication known as scalded skin syndrome can develop. In breastfeeding women, Staph can result in mastitis resulting in inflammation of the breast or an abscess of the breast. Staphylococcal breast abscesses can release bacteria into the mother's milk.
Staphylococcal pneumonia (staph) predominantly affects people with underlying lung disease and can lead to abscess formation within the lungs. Infection of the heart valves (endocarditis) can lead to heart failure. Spread of Staphylococci or staphylococcus (staph) to the bones can result in severe inflammation of the bones known as osteomyelitis. Taphylococcal sepsis is a widespread infection of the bloodstream and is a leading cause of shock and circulatory collapse, leading to death, in people with severe burns over large areas of the body.
Toxic shock syndrome is an illness caused by toxins secreted by Staph aureus bacteria growing under conditions in which there is little or no oxygen. Toxic shock syndrome is characterized by the sudden onset of high fever, vomiting, diarrhea, and muscle aches, followed by low blood pressure or hypotension, muscle aches, seizures and headache which can lead to shock and death. There may be a rash resembling sunburn, with peeling of skin. Toxic shock has been linked to the use of certain types of tampons and less often, to skin wounds and surgery.
Staphylococcal (staph) food poisoning is an illness of the bowels that causes nausea, vomiting, diarrhea, and dehydration. It is caused by eating foods contaminated with toxins produced by Staphylococcus aureus. Symptoms usually develop within one to six hours after eating contaminated food and include abdominal cramps, nausea, vomiting and diarrhea. The illness usually lasts for one to three days. Patients with this illness are not contagious, since toxins are not transmitted from one person to another. The illness can be more serious and last longer in children and older adults.
Septic arthritis is often caused by a staph infection. The bacteria usually target the knees, but other joints can be affected, including the ankles, hips, wrists, elbows and shoulders. Staph arthritis can cause swelling and severe pain in the affected joint along with fever and shaking chills.
Community-associated methicillin-resistant staphylococcus aureus (CA-MRSA) can cause skin infections or a deadly pneumonia. Signs and symptoms, which are similar to those of other types of pneumonia, include cough, shortness of breath and chest pain, but the bacteria also cause massive inflammation and destruction of lung tissue.
In cases of minor skin infections, staphylococcal infections are usually diagnosed by their appearance without the need for laboratory testing. More serious staphylococcal infections such as infection of the bloodstream, pneumonia, and endocarditis require culturing of samples of blood or infected fluids. The laboratory establishes the diagnosis and performs special tests to determine which antibiotics are effective against the bacteria.
A serious concern is when staph infections no longer respond to common antibiotics. Although most staph infections can still be successfully treated, methicillin-resistant staphylococcus aureus (MRSA) is a particularly dangerous and drug-resistant form of staph infection called MRSA appeared in hospitals. MRSA infections often begin as a superficial skin problem that can resemble a pimple or spider bite, but which can quickly turn into a deep, painful abscess that requires surgical draining.
Pseudomonas infections are caused by a bacterium Pseudomonas aeruginosa, which is present throughout the world in soil, water, and on the skin of animals and people. Pseudomonas aeruginosa favors moist areas, such as sinks, toilets, pools, and hot tubs, and usually can withstand standard levels of pool chlorination.
Pseudomonas infection can be sudden and severe, or slow in onset and cause little pain. Pseudomonas infections can infect the blood, skin, bones, ears, eyes, urinary tract, heart valves, and lungs. In most cases, however, pseudomonas infections strike only persons who are very ill, usually hospitalized. Pseudomonas infections rarely cause disease in healthy persons, but can infect those who are already sick or who have weakened immune systems. Pseudomonas aeruginosa are opportunistic pathogens or organisms that do not ordinarily cause disease, but multiply freely in persons whose immune systems are weakened by illness or medication. Patients with AIDS have an increased risk of developing serious pseudomonas infections. Hospitalized patients are another high-risk group, because Pseudomonas aeruginosa are often found in hospitals. Pseudomonas infections can be spread within hospitals by health care workers, medical equipment, sinks, disinfectant solutions, and food. People with diabetes are particularly prone to pseudomonas infections. Furthermore, Pseudomonas aeruginosa is the second most common cause of nosocomial pneumonia and the most common cause of intensive care unit (ICU) pneumonia. Risk factors for acquiring a pseudomonas infection also include having a serious illness or undergoing an invasive procedure such as surgery.
Pseudomonas aeruginosa is a common cause of bacterial infections of the blood and is common in patients with blood cancer and patients who have pseudomonas infections elsewhere in the body. Pseudomonas aeruginosa can infect the heart valves of intravenous drug abusers and persons with artificial heart valves. Persons at risk for pseudomonas infections of the bones and joints include diabetics, intravenous drug abusers, and bone surgery patients. Pseudomonas infections of bones and joints result from direct inoculation of the bacteria or the hematogenous spread of the bacteria from other primary sites of infection. Pseudomonas aeruginosa has a particular tropism for fibrocartilagenous joints of the axial skeleton. Pseudomonas aeruginosa causes chronic contiguous osteomyelitis, usually resulting from direct inoculation of bone, and is the most common pathogen implicated in osteochondritis after puncture wounds of the foot. Pseudomonas aeruginosa can cause inflammation of the tissues covering the brain and spinal cord resulting in meningitis and brain abscesses.
Pseudomonas aeruginosa can cause infections in the external ear canal and is sometimes referred to as swimmer's ear. Pseudomonas aeruginosa can cause serious ear infections in elderly patients, and can cause hearing problems, facial paralysis, or even death. Pseudomonas infections of the eye usually follow an injury and can cause ulcers of the cornea that can cause rapid tissue destruction and eventual blindness. The risk factors for pseudomonas eye infections include: wearing soft extended-wear contact lenses; using topical corticosteroid eye medications; being in a coma; having extensive burns; under-going treatment in an ICU; and having a tracheostomy or endotracheal tube.
Even healthy persons can develop a pseudomonas skin rash following exposure to the bacterium in contaminated hot tubs, water parks, whirlpools, or spas. This skin disorder is also known as pseudomonas skin rash or “hot tub” folliculitis. Pseudomonas blood-borne infections are most often seen in IV drug users. Pseudomonas aeruginosa often invades the blood of people with burns and those who have cancer. Pseudomonas aeruginosa can further cause urinary tract infections, usually in people who have had urologic procedures or those who have an obstruction of the urinary tract. Without treatment, an overwhelming infection can lead to dangerously low blood pressure (shock) and death.
Each of the pseudomonas infections described previously has its own set of symptoms. Pseudomonas bacteremia can cause fever, tiredness, muscle pains, joint pains, and chills. Pseudomonas bone infections can cause welling, redness, and pain at the infected site and possibly fever. Pseudomonas meningitis can cause fever, headache, irritability, and clouded consciousness. Pseudomonas ear infections can be associated with pain, ear drainage, facial paralysis, and reduced hearing. Pseudomonas eye infections can cause ulcers that may spread to cover the entire eye, pain, reduced vision, swelling of the eyelids, and pus accumulation within the eye. Pseudomonas pneumonia can cause chills, fever, productive cough, difficult breathing, and blue-tinted skin. Patients with cystic fibrosis with pseudomonas lung infections can experience coughing, decreased appetite, weight loss, tiredness, wheezing, rapid breathing, fever, blue-tinted skin, and abdominal enlargement. Pseudomonas skin infections can cause a range of symptoms from a mild rash to large bleeding ulcers. Symptoms of pseudomonas folliculitis can include a red itchy rash, headache, dizziness, earache, sore eyes, nose, and throat, breast tenderness, and stomach pain.
Hepatitis is typically caused by hepatitis viruses and can result in inflammation of liver cells and injury to the liver. Hepatitis can also be caused by infections, pregnancy, alcohol, or from herpes simplex virus (HSV), Cytomegalovirus, Epstein-Barr, yellow fever virus, adenoviruses, or Systemic Lupus Erythematosus (SLE). Hepatitis can further be caused from toxins, such as Amanita toxin in mushrooms, carbon tetrachloride, or asafetida. Moreover, hepatitis can also be caused by drugs, such as Paracetamol, amoxycillin, anti tuberculosis medicines, minocycline, methyl-dopa, nitrofurantoin, isoniazide, or ketoconazole.
Mild hepatitis can heal on its own or can progress to more serious hepatitis resulting in scarring of the liver. Acute hepatitis lasts less than six months. Chronic hepatitis lasts longer than six months. Hepatitis can run a subclinical course in which the affected person may not feel ill. However, when the affected person feels sick and symptomatic, hepatitis can impair functions of the liver that include screening of harmful substances, regulation of blood composition, and production of bile to help digestion.
Clinically, the course of acute hepatitis can vary widely from mild symptoms requiring no treatment to fulminant hepatic failure needing liver transplantation. Acute viral hepatitis is more likely to be asymptomatic in younger people. Initial features of acute viral hepatitis can include nonspecific flu-like symptoms, common to almost all acute viral infections and may include malaise, muscle and joint aches, fever, nausea or vomiting, diarrhea, and headache. More specific symptoms, which can be present in acute hepatitis, are: profound loss of appetite, aversion to smoking among smokers, dark urine, yellowing of the eyes and skin, i.e. jaundice, and abdominal discomfort.
For chronic hepatitis, most patients remain asymptomatic or mildly symptomatic. Some chronic hepatitis patients experience symptoms related to acute hepatitis, as well as abdominal fullness from an enlarged liver or spleen, low grade fever and fluid retention. Jaundice can indicate extensive liver damage. Chronic hepatitis patients can have extensive damage and scarring of liver with cirrhosis leads to weight loss and bruising and bleeding tendencies. Chronic hepatitis patients can also have acne, abnormal menstruation, and lung scarring, as well as inflammation of the thyroid gland and kidneys.
Hepatitis A is an infectious jaundice that is caused by a picornavirus. Hepatitis A is often associated with ingestion of contaminated food or with anal or oral sex. It can cause an acute form of hepatitis and does not have a chronic stage. The patient's immune system makes antibodies against hepatitis A that can provide immunity against future infection. People with hepatitis A are advised to rest, stay hydrated and avoid drinking alcoholic beverages. A vaccine is available that will prevent infection from hepatitis A for life. Hepatitis A can be spread through personal contact, consumption of raw sea food or drinking contaminated water. This occurs primarily in third world countries. The time between the infection and the start of the hepatitis A illness can be from 15 to 45 days. Many sufferers of hepatitis A have relapsing symptoms from 6 months to a year following initial diagnosis of hepatitis A.
Hepatitis B is caused by hepatitis B virus (HBV). Cirrhosis of the liver and liver cancer can result from hepatitis B. Transmission of hepatitis B virus (HBV) can result from exposure to infectious blood or body fluids containing blood. Other types of transmission of hepatitis B virus (HBV) can occur from unprotected sexual contact, blood transfusions, re-use of contaminated needles and syringes, and transmission from mother to child during childbirth. A mother who is positive for the hepatitis B surface antigen has a risk as high as 90% if the mother is also positive for the hepatitis B e antigen. HBV can also be transmitted between people by contact of skin or mucous membrane with secretions or saliva containing HBV.
The primary method of transmission reflects the prevalence of chronic hepatitis B virus (HBV) infection in a given area. In low prevalence areas such as the continental United States and Western Europe, where less than 2% of the population is chronically infected with HBV, HBV is typically acquired from injection drug abuse and unprotected sex are the primary methods. In Eastern Europe, Russia, and Japan, where 2-7% of the population is chronically infected, HBV is predominantly spread among children. In high prevalence areas such as China and South East Asia, transmission of HBV often occurs during childbirth.
Hepatitis B virus (HBV) infection can be prevented by vaccination. Infants born to mothers known to carry hepatitis B can be treated with antibodies to the hepatitis B virus (hepatitis B immune globulin or HBIg). When given with the vaccine within 12 hours of birth, the risk of acquiring hepatitis B is reduced 95%. This treatment allows a mother to safely breastfeed her child. Although pharmaceutical products do not typically clear or resolve a hepatitis B infection, they can stop the hepatitis virus from replicating and prevent liver damage such as cirrhosis and liver cancer.
The hepatitis B virus (HBV) primarily interferes with the functions of the liver by replicating in liver cells, known as hepatocytes. During HBV infection, the host immune response causes both hepatocellular damage and viral clearance. Although the innate immune response does not play a significant role in these processes, the adaptive immune response, particularly virus-specific cytotoxic T lymphocytes (CTLs), can contribute to most of the liver injury associated with HBV infection. By killing infected cells and by producing antiviral cytokines capable of purging HBV from viable hepatocytes, CTLs can eliminate the virus. Although liver damage can be initiated and mediated by the CTLs, antigen-nonspecific inflammatory cells can worsen CTL-induced immunopathology, and platelets activated at the site of infection can cause the accumulation of CTLs into the liver.
Hepatitis C virus (HDV) is a blood-borne, infectious, viral disease that is caused by an ahepatotropic virus, known as Hepatitis C virus (HCV). Hepatitis C infection can cause liver inflammation (hepatitis) that is often asymptomatic, but ensuing chronic hepatitis can result later in cirrhosis causing fibrotic scarring of the liver and liver cancer. Hepatitis C virus (HCV) is spread by blood-to-blood contact with an infected person's blood. The symptoms can be medically managed and some patients can be cleared of the virus by a long course of anti-viral medicines. Although early medical intervention is helpful, people with HCV infection often experience mild symptoms, and consequently do not seek treatment. An estimated 150-200 million people worldwide are infected with HCV. In the U.S., those with a history of intravenous drug use, nasally inhaled drug usage, tattoos, or who have been exposed to blood via unsafe sex or social practices are increased risk for HCV. Hepatitis C virus is the leading cause of liver transplant in the United States.
Hepatitis D virus infection can only occur with a concomitant infection with Hepatitis B virus because the hepatitis D virus uses the Hepatitis B virus surface antigen to form a capsid.
In view of the preceding, it is, therefore, desirable to develop safe and successful method (process) and medicinal composition to treat herpes, pseudomonas, hepatitis, staph (staphylococci) and help treat or alleviate cold sores, rashes, skin conditions, or symptoms resulting from herpes, pseudomonas, staph, and hepatitis.